RNA sequencing and conditional Nova mutants reveal that Nova protein function is necessary for activity-dependent alternative splicing of synaptic genes within somatostatin cortical interneurons and regulates its afferent and efferent connectivity.

The importance of synchronous Purkinje cell complex spikes for controlling cerebellar output was investigated by simultaneously recording from cerebellar nuclear cells and arrays of Purkinje cells that synapse onto them.

Despite relative impermeability of the blood-brain barrier for calcitonin gene-related peptide antibodies used in migraine treatment, these antibodies induce certain and highly specific brain effects particularly in the hypothalamus which may be part of the mechanism of their efficacy.

In response to neuronal activity in vivo, mitochondria in dendrites of excitatory neurons inhibit recruitment of ionotropic glutamate receptors through a reactive oxygen signaling mechanism.

Activity-dependent neurite outgrowth and neuronal migration interact to shape modular mesoscale network architecture by homeostatic self-organization.

Notch ligands expressed in the same cell as the Notch receptor are crucial to prevent accidental, ligand-independent Notch activity.

Feedback signaling between the synapse and nucleus via FGF22 and IGF2 directs the activity-dependent stabilization of presynaptic terminals in the mouse hippocampus.

RNA sequencing and genetic mouse models reveal that transcriptional changes to astrocytes in the developing cortex are not intrinsic but influenced by their environment and determine that expression of astrocyte synapse-regulating genes and neuronal synaptogenesis is modulated by ongoing astrocyte-neuron communication.

Hypothalamic stress effector neurons rapidly change activity patterns via recurrent inhibition, representing state-dependent activity switch between baseline and elevated stress levels.

Cohesin is required for the expression of neuronal genes that engage in long chromatin loops, while short-range enhancer-promoter loops can form in the absence of cohesin.